Nevertheless, evidence from cardiology in human patients shows that several cardiac conditions (particularly degenerative mitral valve disease, aortic stenosis, and atrial fibrillation) are accompanied by increased concentrations of antifibrinolytic factors (including PAI‐1 and thrombin activatable fibrinolysis inhibitor [TAFI]) which collectively decrease endogenous fibrinolytic activity and promote prothrombotic states [63, 64]. The gene discussed is CPB2; the disease is atrial fibrillation.